Positively-charged chrysotile asbestos binds to and distorts red blood cell membranes. Using negatively-charged particles and the thiobarbituric acid (TBA) assay for N-acetyl neuraminic (sialic) acid, we have added new data to directly support the hypothesis that hemolysis is mediated through interactions between positively charged asbestos and cell membrane glycoproteins. Five sets of experiments have been completed: 1) Chrysotile and crocidolite asbestos cause over 85% of red blood cells (RBCs) to become distorted only 5-15 min. after treatment. 2) Neuraminidase protects over 85% of the RBCs from the distorting affects of chrysotile, but not crocidoliate asbestos. 3) Treatment of RBCs with chrysotile, but not crocidolite asbestos, caused alterations in the distribution and number of lectin-labeled gold spheres on cell surfaces. 4) The TBA assay showed that asbestos treatment did not cause a release of sialic acid into the medium. Neuraminidase removed over 85% of the sialic acid from normal cells in 3.5 hrs. Chrysotile, but not crocidolite asbestos, prevented the removal of 70% of the sialic acid by neuraminidase. 5) Intracellular analysis of Na+:K+ ratios showed that chrysotile, but not crocidolite asbestos, caused significant abnormal ion flux within 5-15 min. after treatment. These experiments strongly support the hypothesis that chrysotile asbestos causes membrane damage through binding to terminal sialic acid residues. Similar studies with pulmonary cells such as macrophages, epithelial cells and fibroblasts will attempt to elucidate the mechanisms through which inhaled asbestos causes cell damage in vivo.